Sialic acid, released from milk glycans, has been identified as a primary carbon source driving increases in populations of Enterobacteriaceae and Clostridiaceae, which leads to diarrhea in nursing mammals. Data has demonstrated that the bacterial sialidases liberate sialic acid which is consumed by populations of Enterobacteriaceae in the gastrointestinal tract of nursing pigs. This sialic acid is released from milk glycans and host glycans by a bacterial enzyme, sialidase also known as neuraminidase (EC 3.2.1.18). The present technology demonstrates the reduction in sialic acid and N-acetylglucosamine, by delivery of an organism which consumes sialic acid, sialic acid-containing milk glycans, N-acetylglucosamine, or N-acetylglucosamine-containing milk glycans to limit available concentrations of these glycans in vivo. Specifically, this research has shown that this reduction is effective in preventing colonization by these pathogens in nursing animals through this mechanism. Evidence for reduction of Enterobacteriaceae by sialic acid consuming lactobacillus is presented.
There are currently no methods which selectively prevent or reduce the growth of Enterobacteriaceae populations in the gut of animals by reducing their nutritional niche in the gut. Piglet diarrhea (scour) and populations of Enterobacteriaceae and Clostridiaceae are controlled at present by antibiotics or vaccines, which do not selectively inhibit the populations of Enterobacteriaceae and prevention strategies.